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Doctoral Projects Master's Theses and Graduate Research

Spring 4-2017

Developing a Clinical Tool for the Assessment and Diagnosis of Developing a Clinical Tool for the Assessment and Diagnosis of

Pediatric Bipolar Disorder Pediatric Bipolar Disorder

Amanda Jill Horrocks California State University, Northern California Consortium Doctor of Nursing Practice

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Recommended Citation Recommended Citation Horrocks, Amanda Jill, "Developing a Clinical Tool for the Assessment and Diagnosis of Pediatric Bipolar Disorder" (2017). Doctoral Projects. 58. DOI: https://doi.org/10.31979/etd.9ry3-6ynm https://scholarworks.sjsu.edu/etd_doctoral/58

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ABSTRACT

Developing a Clinical Tool for the Assessment and Diagnosis of Pediatric Bipolar

Disorder Background: Pediatric bipolar disorder is a significant mental illness,

characterized by changes in mood that can be abrupt, unpredictable, and extreme. The

rate of diagnosis of this disorder has been increasing in recent decades. Purpose: A

thorough review of existing literature was completed to inform practice. Additionally, a

survey of clinician assessment practices was completed. Combining the information

learned from the literature review, and the data from the clinician survey, a clinical tool

has been created. This tool provides a thorough, multi-phasic process for the assessment

and diagnosis of pediatric bipolar disorder. Method: Mental health clinicians were

surveyed; respondents were obtained via snowball sampling. Chi square analysis was

completed to determine the relationships between the assessment practices used and the

level of licensure of the clinician, the length of time the clinician had been in practice,

and the age range treated by the clinician. Results: No statistically significant results

were identified from the Chi Square analyses. Inconsistency in the assessment strategies

was noted, however. Implications/Conclusions: Further clinician data should be

obtained due to the small sample size (n=16). The resulting tool has been reviewed by a

subject matter expert and will be validated in practice before diffusion.

Amanda Jill Horrocks, DNP(c), RN, PMHNP-BC

April 2017

DEVELOPING A CLINICAL TOOL FOR THE ASSESSMENT

AND DIAGNOSIS OF PEDIATRIC BIPOLAR DISORDER

by

Amanda Jill Horrocks, DNP(c), RN, PMHNP-BC

A project

submitted in partial

fulfillment of the requirements for the degree of

Doctor of Nursing Practice

California State University, Northern Consortium

Doctor of Nursing Practice

April 2017

APPROVED

For the California State University, Northern Consortium Doctor of Nursing Practice:

We, the undersigned, certify that the project of the following student meets the required standards of scholarship, format, and style of the university and the student's graduate degree program for the awarding of the doctoral degree. Amanda Jill Horrocks, DNP(c), RN, PMHNP-BC

Project Author

Ruth Rosenblum, DNP, RN, PNP-BC, CNS Nursing Chairperson's name (Chair) San Jose State University

Michael Terry, DNP, RN, FNP, PMHNP Nursing Committee member's name University of San Diego

AUTHORIZATION FOR REPRODUCTION

OF DOCTORAL PROJECT X I grant permission for the reproduction of this project in part or in

its entirety without further authorization from me, on the condition that the person or agency requesting reproduction absorbs the cost and provides proper acknowledgment of authorship.

Permission to reproduce this project in part or in its entirety must

be obtained from me. Signature of project author: Amanda Jill Horrocks, DNP(c), RN, PMHNP-BC

ACKNOWLEDGMENTS

I would like to thank Dr. Ruth Rosenblum, Dr. Michael Terry, and Dr.

Jason Earle for your support and guidance with this project. Your presence and

input has been invaluable. Mom and Dad, thank you for your incessant support.

Carter, Stuart, Gabriel, and Sebastian, you light up my life and bring me so much

joy! Thank you to my family and friends who have stood by me, and encouraged

me during this endeavor. AMDG +

TABLE OF CONTENTS

Page

LIST OF TABLES .................................................................................................. vi

CHAPTER 1: INTRODUCTION ............................................................................ 1

CHAPTER 2: LITERATURE REVIEW ................................................................. 6

CHAPTER 3: METHODOLOGY .......................................................................... 21

CHAPTER 4: RESULTS ....................................................................................... 25

CHAPTER 5: DISCUSSION ................................................................................. 27

REFERENCES ....................................................................................................... 34

APPENDICES ........................................................................................................ 43

APPENDIX A: GLOSSARY OF TERMS ............................................................. 44

APPENDIX B: CLINICIAN SURVEY ................................................................. 48

APPENDIX C: CLINICIAN DATA TABLES ...................................................... 55

APPENDIX D: CLINICAL TOOL ........................................................................ 57

APPENDIX E: PERMISSION FOR USE.............................................................. 66

LIST OF TABLES

Page

Table 1. Assessment Strategies Employed ............................................................. 56

Table 2. Family Screening…………………………………………………..……56

CHAPTER 1: INTRODUCTION

Background

Bipolar disorder (BPD) is a serious mental health condition characterized by

recurrent periods of depression and elevated mood; these mood shifts are accompanied by

cognitive and behavioral symptoms (Anderson, Haddad, & Scott, 2012). Dilsaver (2011)

reported an estimated lifetime incidence of bipolar spectrum disorders is between 4.4%

and 6.4%. Pediatric BPD is becoming more prevalent in the United States (US); in 1996

BPD was the least common diagnosis for children receiving inpatient psychiatric care,

and by 2004 it was the most common (Littrell and Lyons, 2010). Contributing factors to

this rise in diagnosis include an expansion of criteria to include a spectrum of BPD’s, and

a greater understanding of the genetic heritability of the condition (Littrell & Lyons,

2010). The incidence rate of BPD in the pediatric population is approximately 2%

(Youngstrom, Jenkins, Jensen-Doss, & Youngstrom, 2012).

Across the lifespan, the implications of BPD are more significant than the other

disorders that have similar clinical presentations, like attention deficit hyperactivity

disorder (ADHD) or oppositional defiant disorder (ODD). Goldstein (2009) reported a

lifetime rate of suicidal ideation of up to 75%, a 44% suicide attempt rate, and a

completed suicide rate of 25% for those with BPD. BPD is also known to be a kindling

illness, making an accurate diagnosis and early treatment important (Weiss et al., 2015).

Kindling refers to the phenomenon whereby the experience of life stress causes mood

cycles to exacerbate in individuals suffering from conditions like BPD (Weiss, et al.,

2015).

2 Purpose

The purpose of this project was to complete a thorough review of existing

literature about pediatric BPD, to conduct a survey amongst mental health clinicians, and

use the information and data obtained from these processes, to create a clinical tool for

the assessment and diagnosis of pediatric BPD. Literature has been reviewed to provide

an evidence-based foundation for the development of the tool. Clinicians were queried

and their responses analyzed to determine the level of licensure, the length of time in

practice, age ranges treated, and assessment strategies employed. Research questions

analyzed were:

1) Is there a significant difference between the type of licensure that a clinician holds

and the assessment strategies used in clinical practice?

2) Is there a significant difference between the length of time a clinician has been in

practice and the assessment strategies used in clinical practice?

3) Is there a difference between the age ranges that clinicians treat and the

assessment strategies used in clinical practice?

Youngstrom, Jenkins, Jensen-Doss, and Youngstrom (2012) proposed several

evidence-based steps that could be followed to assess pediatric BPD, but failed to

incorporate a tool that could be used or medical screening elements. This project created

a process that will incorporate clinical interviewing, obtaining collateral data, completing

valid and reliable screening tools, and obtaining diagnostic studies before assigning this

diagnosis. It is expected that the robust nature of the screening tool will allow for rapid

adoption of the process by clinicians (Dearing, 2009).

3 Current assessment practices to diagnose pediatric BPD are often subjective,

inconsistent, and do not follow a cohesive, researched process (Jenkins, Youngstrom,

Youngstrom, Feeny, & Findling, 2011). Additionally, these authors noted that BPD,

compared to other conditions, is more challenging to accurately diagnose due to the

varying mood states in which a patient may present (Jenkins et al., 2011). A patient with

Bipolar I disorder, for example, may present for treatment in full mania, hypomania,

euthymia, dysthymia, severe depression, or a mixed state. Clinicians should conduct

thorough interviews, and incorporate valid screening tools to assist in making a BPD

diagnosis. It is also important to incorporate evidence-based, objective methods of

assessment to reduce diagnostic ambiguity. Accurate, early identification and treatment

will yield more positive patient outcomes due to the initiation of earlier treatment

(Maniscalco & Hamrin, 2008).

It is thought that in some situations pediatric BPD is over diagnosed, and in other

scenarios, it is misdiagnosed as another condition (Danner et al., 2009). Several pediatric

mental health conditions have overlapping symptoms (Youngstrom, Birmaher, &

Findling, 2008), and consequently, this makes accurate diagnosis challenging.

Youngstrom et al. noted that irritable mood, distractibility, and pressured speech are

common in pediatric BPD, but that these symptoms are not sensitive to the condition.

Conduct disorder (CD), ODD, and ADHD all share symptoms in common with pediatric

BPD, and they can be mistaken for each other clinically (Danner, et al., 2009).

Post et al., (2015) noted that there is a life expectancy loss of 13-30 years in

individuals who have a serious mental illness. BPD is considered serious mental illness,

according to DeHert et al., (2011). BPD is a costly public health issue, Dilsaver (2011)

4 noted that the economic burden of bipolar I and bipolar II disorders is 151 billion dollars

in the US annually. The significance of these statistics provides support for the diffusion

of the clinical tool as an innovative clinical process. The degree to which the tool can

help to change these statistics should be highlighted to increase the likelihood of adoption

by clinicians. The tool represents an innovation to enhance current assessment strategies,

and the diffusion of the attributes of the tool will aid clinicians in adopting the new

process (Dearing, 2009).

Theoretical Framework

Diffusion of innovation theory provides a foundation and guide for the execution

of this project. This theory involves taking the innovative idea of the clinical tool, and

diffusing its content and use to clinicians, the clinicians choosing to accept the innovative

process, and clinicians adopting the innovation into practice (Dearing, 2009). The

beneficial attributes of the process must be readily identified by clinicians to aid in their

ease of adoption. Information regarding the evidence-based assessment strategies

incorporated, and rationale behind the recommendations for the innovative aspects of the

tool will have to be diffused to clinicians to aid in their adoption process (Dearing, 2009).

The theory suggests that accelerated diffusion of concepts, and thus accelerated adoption

of the innovation can be achieved by incorporating validated concepts (Dearing, 2009).

The clinical tool has achieved this by clustering together several evidence-based

assessment strategies for the first several phases of assessment.

Murray (2009) discussed the application of the diffusion of innovation theory to

psychotherapy practice. Murray reviewed the major tenets of the theory, and ultimately

discussed that clinicians will more readily adopt the innovation into practice if they find

5 the research meaningful to their clinical work (Murray, 2009). The clinical tool was

developed with this in mind. Training and dissemination efforts will need to focus on

ensuring clinicians can recognize the value of the new process, as well as its ease of use

and adoption clinically.

CHAPTER 2: LITERATURE REVIEW

Assessment and Diagnosis

Youngstrom, Jenkins, Jensen-Doss, and Youngstrom (2012) reviewed evidence-

based assessment strategies used to diagnose pediatric BPD. The authors provided an

algorithm of steps that could be used to assess for this condition, as well as a figure

diagramming the use of these steps. There was no tool or manner in which the presented

process should be applied in the clinical setting. Some similarities include the inclusion

of several commonly utilized evidence-based assessment strategies. Some of the

differences include that the authors of the article provided some steps in their process to

use after a diagnosis of BPD had been assigned; the tool focuses on ruling in or ruling out

the diagnosis. Another difference is that the created clinical tool includes

recommendations for laboratory and imaging studies.

Algorta et al. (2013) completed a non-experimental, correlational study with a

brief screening tool, the Family Index of Risk for Mood Issues (FIRM), to enhance the

accuracy of pediatric BPD diagnoses. This study and resulting tool is aligned with one of

the steps that is proposed by Youngstrom, Jenkins, Jensen-Doss, and Youngstrom (2012).

It does not, however, give a comprehensive process for assessment, but provides a helpful

tool for the clinician to use as a part of the process. The sample included pediatric

subjects aged 5-18 years (average 10.3 years), and their caregivers. All subjects were

seeking an outpatient psychiatric evaluation. Subjects came from 273 families, from

these families, 43 youth were found to be on the bipolar spectrum. Caregivers completed

the Mood Disorder Questionnaire – Parent (PMD-Q), and the FIRM appeared at the end

of the PMD-Q. Caregivers also completed a Child Behavior Checklist (CBCL) about the

7 youth subject. Youth subjects were assessed with the Kiddie Schedule for Affective

Disorders and Schizophrenia – present and lifetime (K-SADS-PL), supplemented with

other interview questions. Guardians were assessed for mental health history and were

administered a Mini International Neuropsychiatric Interview (MINI). Logistic

regression was completed to determine if FIRM provided a significant improvement in

the identification of BPD. A t-test was also completed to establish if any test performed

significantly better than another. The FIRM was more sensitive to BPD than other tools

and did not correlate to ADHD. The logistic regression showed that FIRM provided a

significant improvement in detecting BPD. An identified strength of this study was that

the subjects were all assessed in a thorough manner by highly trained research assistants.

An identified limitation of the study was that the demographic characteristics of the

study, with 90% of subjects being from low-income families, likely reduced the

effectiveness of the FIRM. This study is important to this project as it discussed the

FIRM, which is an effective yet easily administered screening tool for the presence of

BPD. The FIRM is included in the resulting tool of this clinical project for its ease of use

and effectiveness.

Providing additional support to the previous two articles, Martelon, Wilens,

Anderson, Morrison, and Wozniak (2012) completed a case-control family study to

explore the link between challenges in the gestational and neonatal periods with the

development of pediatric BPD. Subjects were obtained from two other ongoing similarly

designed studies. There were 98 healthy controls, 120 bipolar patients, and 120 non-

affected siblings included. Subjects under the age of 18 were assessed using the K-SADS

– epidemiologic version (K-SADS-E), and those 18 and older were assessed with the

8 Structured Clinical Interview for DSM-IV (SCID). Mothers of all subjects completed a

module of the Diagnostic Interview for Children and Adolescents – Parent Version

(DICA-P). Statistical analyses included Chi square and t tests. A significant relationship

was found between BPD and neonatal challenges. No significant relationship was found

between gestational challenges and the development of BPD. One limitation of this study

is the fact that the DICA-P was completed retrospectively, and there is a chance that

mothers may not accurately remember the significance of any challenges with their

pregnancy or the neonatal period. This study is important to this project as it re-enforces

the need to have a thorough gestational, neonatal, and pediatric history obtained during

the clinical interview. Both Algorta et al. (2013) and Youngstrom, Jenkins, Jensen-Doss,

and Youngstrom (2012) discussed the importance of understanding family history as a

part of the assessment process.

Moving away from the process of assessment into the diagnosis itself, Hafeman et

al. (2013) conducted a non-experimental, case-control study to determine if youth

diagnosed with BPD, not otherwise specified (NOS) were similar to those with BPD I or

BPD II. The sample included 707 children with a mean age of 9.4 years, presenting for

treatment at an identified outpatient clinic. The subjects were evaluated and diagnosed

with BPD I (n=71), BPD II (n=3), BPD NOS (n=88), or no BPD (n=545). Subjects were

assessed using the K-SADS-PL, young mania rating scale (YMRS), K-SADS Depression

Rating Scale, K-SADS Mania Rating Scale (KMRS), and the Children's Global

Assessment Scale (CGAS). BPD II was eliminated from the analysis due to the low

number of subjects with that diagnosis. Analysis of variance (ANOVA) testing was

completed for continuous variables, and Chi square testing for the categorical variables,

9 to determine differences between the three remaining groups. BPD NOS showed no

significant difference from BPD I in mood symptoms at baseline. BPD NOS had lower

KMRS than BPD I, but both had significantly elevated scores when compared to no BPD.

CGAS also showed significant impairment in BPD NOS and BPD I compared to no

BPD. An identified strength of this study was the thorough diagnostic assessment given

to the subjects, including a myriad of validated assessment tools. This study is important

to this project as it discussed the similarity in the clinical presentation for different

diagnoses across the BPD spectrum.

Providing a different perspective, Benti, Manicavasagar, Proudfoot, and Parker

(2014) conducted a qualitative study with a phenomenological approach to understand

the early experiences of patients with BPD, and how they differed from those diagnosed

with unipolar depression (UD). Some controversy still exists about diagnosing BPD in

the pediatric population, and this study provided some information about individuals

living with BPD. There were 39 participants aged 18-35 years old; all were diagnosed

before age 24. Twenty participants had UD and 19 had BPD. All participants were given

the MINI, YMRS, and the Hamilton Rating Sale for Depression (HAM-D) by the same

clinician to determine that they were in a state of euthymia at the time of the study. After

determining that they were eligible to participate based on diagnosis, age, and mood state,

the participants completed a semi-structured interview. Descriptive statistics were

obtained for the demographic data of participants. There was a trend noted for a younger

age of onset in BPD than in UD. Indicators for BPD that were revealed included: adverse

home environments, more assertive and disinhibited personalities, and mood swings at a

young age. This study is important to the project as it gives insight to the age and nature

10 of the onset of symptoms. This article provides support for the diagnosis and early

treatment of BPD, based on the experiences of the subjects.

Similar to Benti, Manicavasagar, Proudfoot, and Parker (2014), Carpenter-Song

(2009) completed a qualitative study with an ethnographic focus, to learn about the lived

experience of patients and families dealing with mental health issues. One primary

difference from the preceding article is that the previous study involved the patients

recounting their earlier experiences, whereas Carpenter-Song studied pediatric patients

and their families while they were still children. There were 20 families in the study: nine

African American, ten Euro-American, and one Latino. The socioeconomic statuses of

the families ranged from upper middle class to low income. Nineteen children in the

study met criteria for BPD spectrum or ADHD. Youth were evaluated using the K-

SADS-PL to determine their diagnosis for the study. A semi-structured interview, the

Subjective Experience of Illness and Medications in Youth was used to evaluate

participants. Interviews were conducted in participant homes over multiple sessions.

The study included detailed descriptions of three families and provided some of their

responses to questions about their lived experience. The medicalization of these

conditions was discussed, along with the participant's experiences with providers. An

identified strength of this study is the ethnographic approach that is not taken into

account in many quantitative studies. It is possible that families, like the described

African American families in this study, would not participate in some other quantitative

research because they do not attribute these mental health concerns to individual

pathology. Having all perspectives considered and reported gives strength to this data

and the study. This study is useful for this project as it discussed the lived experience of

11 patients and families involved in the mental health system. Additionally, it discussed

important cultural considerations regarding attitudes about mental illness that are

important to consider. Families who do not believe in mental illness or sense stigma

about seeking care might be less likely to seek help or discuss troubling symptoms.

Neurobiological Changes

Chang et al. (2005) conducted a case-control study to examine structures of the

limbic system in patients with BPD and healthy controls. Twenty children and

adolescents with BPD were recruited from an ongoing study. Each of the subjects had a

gender, age, and IQ-matched control recruited from the community. SCID, K-SADS,

and K-SADS-PL were used to evaluate subjects. Bipolar patients were additionally

evaluated with the YMRS. T-tests were used to analyze the data obtained from magnetic

resonance imaging (MRI) studies. No statistical significance was seen between BPD

subjects and controls for total brain volume, thalamus, caudate, and hippocampus. Total

amygdalar volume, as well as right and left amygdalar volume was significantly

decreased in the BPD subjects. Further study showed this reduction to be related to

depletion of gray matter volume (GMV) in the right amygdala. Treatment with lithium

or valproic acid was shown to be somewhat protective of this change. This study

provides support for this project in that it demonstrates underlying neurobiological

processes that appear to be a part of the BPD presentation. It also supports that treatment

of BPD can be protective against this neurobiological change; an important consideration

when considering diagnosing BPD in the pediatric population.

Similar to Chang et al. (2005), Lisy et al. (2011) conducted a study that found

changes in GMV in MRI scans of patients with BPD. Additionally, both studies had

12 findings showing that treatment with certain medications for BPD is brain protective.

Lisy et al. completed a longitudinal case-control study to assess changes in GMV in

subjects with BPD and healthy controls. Fifty-eight subjects with BPD and 48 healthy

controls underwent a baseline MRI scan, and then a follow-up scan some months later

(mean of 11months). Assessments were completed using the K-SADS and the SCID

based on the age of the subject. BPD patients were in a variety of mood states at the time

of their baseline MRI. Healthy controls were found to have greater gray matter volume

compared to BPD patients overall. BPD patients, however, had increased gray matter

volume over time. There was a positive correlation in the bipolar group between the

length of time between scans and the change in gray matter volume. BPD patients

receiving antipsychotics or anticonvulsants showed increases in the left frontal gyrus and

the left medial gyrus, respectively. This study did not note a change in GMV between

scans in patients receiving lithium. The longitudinal nature of this study is a strength.

One limitation of this study is that subjects with nicotine dependence were not excluded

from participation, and this has been linked to GMV changes in the past. This study is

important to the project as it demonstrated neurostructural changes related to BPD.

Different from the preceding two studies, Xiao et al. (2013) conducted a case-

control study to determine neurologic changes of manic pediatric BPD patients. Lisy et

al. (2011) included patients in a variety of mood states, whereas Xiao et al. included only

manic patients. The study by Xiao et al. included 15 patients aged 12 to 17 years old

from outpatient psychiatric clinics in China, and they were age and sex matched with

healthy controls. Subjects met criteria for BPD, had to have one previous manic or

hypomanic episode, and were manic at the time of completing the study. Participants

13 were evaluated using the K-SADS-PL, and the Wechsler Abbreviated Scale for

intelligence. BPD patients additionally completed the YMRS. Statistical analysis was

completed using Chi square tests and t tests. MRI scans were completed, and changes

were found in the bilateral hippocampus, right anterior cingulate cortex, right

parahippocampal gyrus, and left caudate. Chang et al. (2005) did not find changes in the

caudate or hippocampal structures like this study did. Some of this could be related to

differences in study design. This study demonstrated neurobiological changes that can be

observed during the resting state, and during task completion in BPD. This study is

important to the project as it outlines some of the neurobiological changes that can be

appreciated in the brain of the bipolar patient compared to a healthy control when there

was no task being completed. This information suggests that objective findings might be

possible when diagnosing pediatric BPD.

Exploring a different aspect of neurobiological function in BPD, Quiroz, Gray,

Kato, and Manji (2008) completed a retrospective review to examine the role of

mitochondrial function in BPD. The authors noted evidence is emerging that

mitochondria play a role in the ability for neurotransmitters to freely move between

neurons. Dysfunction in calcium transportation and utilization is another anomaly that

has been documented in BPD; this could also be linked to mitochondrial function. Over

12,000 hippocampal genes from autopsied brains of patients with BPD, schizophrenia,

and healthy controls were analyzed. Forty-three genes were expressed in a diminished

manner for BPD as opposed to schizophrenia. Forty two percent of these changes were

related to mitochondrial function. It was noted that treatment with lithium and valproic

acid were protective to brain function, similar to the other studies discussed that

14 completed MRI scans. This article is important to the project as it explored the biologic

basis for BPD.

Susceptibility Genes and Genetic Linkage

Lichtenstein et al. (2009) conducted a population-based retrospective study to

assess heritability and environmental factors that contribute to susceptibility for

schizophrenia, BPD, or a comorbidity of both conditions. The sample was obtained by

linking national registries. Over nine million potential participants were identified, and

the article stated that over 2 million families were analyzed. Rates of disease in family

members was compared to those with hospitalizations who were the same age and

gender. Different family types were analyzed in an attempt to separate genetic from

environmental factors for susceptibility. A generalized multivariate mixed linear model

was used. Heritability of schizophrenia was estimated to be 64%, and BPD was

estimated to be 59%. An identified limitation was that the data used to determine the

sample was the lack of information about the diagnostic practices of the treating

clinicians. Additionally, they may not utilize a standardized approach to the assessment

of BPD and did not know that their assigned diagnoses would be used for the purpose of

this study. This study supports this project as it demonstrated the high rate of heritability

of BPD, warranting consideration of the genetic factors during the assessment of

potential BPD cases.

Different from Lichtenstein et al. (2009), Barden et al. (2006) completed a case-

control study to examine three different specific genes as potential factors leaving one

susceptible to developing BPD. The genes studied were: purinergic receptor P2X 7

(P2RX7), purinergic receptor P2X 4 (P2RX4), and calcium/calmodulin dependent protein

15 kinase kinase 2 (CAMKK2). Two hundred thirteen individuals from Quebec were

identified using the French version of SCID. There were 214 control subjects. Blood

samples were obtained from all subjects. Fisher’s exact tests were used to analyze data.

Single nucleotide polymorphism’s (SNP) associated with P2RX7 accounted for 56% of

all SNP’s in this genetic area. All three genes studied are implicated in the synaptic use

of calcium and subsequent modulation of neurotransmitters. The data obtained from this

study suggest susceptibility to BPD may exist through P2RX7 and CAMKK2, though

stronger in the former. There was a significant association between 2 markers of P2RX7

in BPD as compared to control subjects. The authors also suggested that due to the space

between implicated susceptibility genes, there may be a gene cluster associated with

BPD. This study is important to this project as it gives discussion to the biological basis

of BPD, and offers some genetic markers that may be implicated in the development of

BPD.

Doyle et al. (2010), explored genetic susceptibility to BPD, and like Barden et al.

(2006), found some genes suggestive of playing a role in the development of the disorder.

Doyle et al. additionally explored the heritability of BPD. The authors completed a non-

experimental, correlational descriptive study to expand on previous research regarding

the diagnosis and genetic basis of pediatric BPD. Subjects were obtained from a group

previously studied in a sibling-pair linkage ADHD project. Subjects aged 6-17 years old

were assessed using the K-SADS-E, and subjects 18 years old and older were assessed

with the SCID. Weschler Intelligence Scales (IQ) were completed for all subjects as

well. A CBCL was completed by guardians of subjects aged 6 to 18 years. Genotyping

was then completed on the subjects. Youth with CBCL data were the focus on of the

16 main analysis. The independent variable was the youth with the juvenile BPD phenotype

based on the CBCL scores (CBCL-JBD). Heritability for CBCL-JBD was found. The

genomic scans revealed suggestive linkage for youth with CBCL-JBD at 1p21.1 (changes

with chromosome 1), 6p21.3 (changes with chromosome 6), and 8q21.13 (changes with

chromosome 8), though no genetic markers had a statistically significant correlation to

the phenotype. An identified limitation of this study was that only 54% of CBCL were

returned. This study is important to the project because it discussed the heritability of

BPD, and found some suggestive susceptibility genes, though statistical significance was

not found.

Another exploration of genetic susceptibility for BPD was completed by Jang et

al. (2015), who completed an animal study on transient receptor potential cation channel

subfamily M member 2 (TRPM2) deficient mice, to explore the biologic basis of BPD in

humans. Many behavioral tasks were completed and video recorded. Mice also

underwent electroencephalogram studies and blood tests. Animal handling protocols

were followed, and this study was completed in Korea. One way ANOVA tests were used

to analyze data obtained. This study examined the changes associated with three

mutations of TRPM2. One particular mutation, D543E demonstrated significant changes

in behavior and function. Having these mutations leads to an inappropriate production of

other proteins naturally occurring in the brain. One of these, GSK-3, is known to be

directly related to mood regulation. The nature of this study being an animal study with

interwoven knowledge of human BPD is both a strength and weakness. The strength lies

in the intricate and robust study that was completed, but the weakness is that this has not

been replicated fully in the human population. This study is important to this project by

17 providing information that could be directly related to the development of BPD in

humans.

Olivera et al. (2014) explored the genetic factors related to BPD development

from a different perspective. The authors conducted a non-experimental, case-control

study to determine if there was a genetic response to infection or inflammation that leaves

one susceptible to the development of BPD. DNA from 571 French patients with BPD

(229 early onset before age 22, and 342 late onset), and 199 healthy controls were

analyzed for toll-like receptor 2 (TLR2) polymorphisms. All subjects were euthymic at

the time of inclusion, as evidenced by completion of a Montgomery-Asberg Depression

Rating Scale and a Mania Rating Scale. The independent variable was the presence of

BPD, and the dependent variables were the presence or absence of TLR2 polymorphisms.

Genotype frequencies between the early onset, late onset, and healthy controls were

performed using Chi square tests. The TLR2 rs380499 TT and TLR2 rs4696480 TT

genotypes were found to be significantly more present in early onset BPD patients than

late onset. No statistically significant difference was found between the late onset group

and the healthy controls. An identified strength of this study was the homogenous

sample and a large number of sample subjects. This study is relevant to the project as it

provides information regarding background questions that should be asked during the

clinical interview, and identified statistically significant susceptibility genes for pediatric

BPD.

Deepening the body of evidence for genetic linkage, Shifman et al. (2004)

conducted a case-control study to explore the association between catechol-O-

methyltransferase (COMT) and BPD. This study was completed in Jerusalem, Israel.

18 There were 217 unrelated case subjects; diagnosis was confirmed with the SCID. All

subjects were of Ashkenazi Jewish descent. Control samples were obtained from around

1,050 healthy Ashkenazi individuals. Chi square tests were completed to analyze data

received. Gender specific samples were run, as a gender effect had previously been

identified with COMT. A significant association was found between SNP’s of COMT

and BPD. Based on previous research, the data of this study also demonstrated a

relationship between schizophrenia and BPD. The size of the control group is a strength

of this study. However, the study does not indicate if these controls were screened. Some

controls may have had BPD and did not know it. Though the strength of the correlation

between COMT and BPD has been found to be more modest in the decade since this

research was completed, this article provides support for the completion of this project

due to the relationship found with both BPD and schizophrenia.

Like other studies in this section, Zhou et al. (2009) completed a study to explore

another potential gene leaving individuals susceptible to developing BPD. Zhou et al.

conducted a study that had a correlational component for European Caucasian families,

and a case-control component for Chinese subjects. The study was conducted to

determine if there was a link between Sp4 transcription factor (Sp4) and BPD, as Sp4 is

known to play a role in hippocampal development in animal studies. Ten SNP’s located

across Sp4 were evaluated. RMANOVA tests were used to analyze the data obtained. 4

SNP's were found to be statistically significant and associated with BPD. The number of

subjects and the fact that results were replicated in two different ethnic groups are

strengths of this study. The article is important for the project because it identifies a

19 susceptibility gene that was found to be statistically significant in a large sample across

ethnic groups.

Gaps in Research

Literature searches were completed in the CINAHL and PsycINFO databases

using the search terms “assessment diagnosis pediatric bipolar disorder,” “assessment

pediatric bipolar disorder,” and “pediatric bipolar disorder.” Additionally, a search was

completed in both CINAHL and PsycINFO for “susceptibility genes bipolar disorder,” as

there is interest in incorporating emerging information regarding genetic polymorphisms

that are related to BPD into this project. Youngstrom, Birmaher, and Findling (2008)

reviewed the sensitivity and specificity of symptoms to BPD and other conditions.

Studies referenced in the literature review often utilized validated rating scales as a part

of the assessment strategy. This is helpful but does not seem substantial enough, as

diagnostic challenges still exist. Rucklidge (2008) found that retrospective completion of

rating scale tools did not reveal prodromal periods for those patients who were diagnosed

after puberty. They did demonstrate symptoms that were indicative of psychopathology,

however. This re-enforces the need for thorough assessment during the childhood and

adolescent years so that treatment onset is not delayed. Kessing, Vradi, and Andersen

(2015) noted that of those diagnosed with pediatric BPD, 40.7% of patients received the

diagnosis at their first point of contact, but 24% of these patients eventually were given a

different diagnosis after follow up.

Faraone, Glatt, and Tsuang (2003) noted that pediatric BPD is often more severe,

and may be under stronger genetic influence than adult onset BPD. Several genes have

been identified as leaving one susceptible to developing pediatric BPD. One of these

20 genes was discussed in the article by Olivera et al. (2014) in the literature review above.

Some of the others include specific polymorphisms of COMT, brain-derived

neurotrophic factor (BDNF), and the dopamine transporter (DAT) (Mick et al., 2008).

Many of these genetic pathways show susceptibility, but none of them provide a direct

pathway to diagnosis based on the current information available. Given the information

available, and considering that no one tool provides a completely reliable pathway to

diagnosis, this project is needed to provide as consistent and clear a path as possible to

diagnosis.

CHAPTER 3: METHODOLOGY

Study Design and Research Questions

The project had several elements: a systematic review of the literature to inform

practice, a survey of clinicians, and the development of a clinical tool that could be

implemented to more thoroughly and consistently assess for pediatric BPD. Research

questions analyzed were:

1) Is there a significant difference between the type of licensure that a clinician holds

and the assessment strategies used in clinical practice?

2) Is there a significant difference between the length of time a clinician has been in

practice and the assessment strategies used in clinical practice?

3) Is there a difference between the age ranges that clinicians treat and the

assessment strategies used in clinical practice?

Sampling and Method

Survey respondents were recruited via snowball sampling; approximately 50-100

respondents were desired to minimize distribution errors in responses (Field, 2013).

Criteria for inclusion required that the respondent be a medical doctor, physician’s

assistant, nurse practitioner, or clinical nurse specialist working in the field of mental

health. Clinicians additionally needed to treat some children or adolescents in their

practice to be included in the survey. Children and adolescents, for this project, were

defined as people aged 3 to 17 years. Clinicians did not have to exclusively treat this age

group and did not need to have any specific portion of their practice be dedicated to the

child and adolescent population. Exclusion criteria are any individuals who did not meet

the aforementioned practice criteria. All subjects were able to provide their informed

22 consent to participate in the survey, and none belonged to a protected category of

subjects. Several published studies explore aspects of the existence, assessment, and

diagnosis of pediatric BPD, but there does not appear to be any published English

literature other than Youngstrom, Jenkins, Jensen-Doss, and Youngstrom (2012) that

address a process for assessment. The similarities and differences between their article

and this work were previously explored in this paper.

Respondent participation was voluntary. The respondents received the link for

the survey from people that they know, due to the snowball sampling methodology. The

potential respondent had the sole ability to click the link and begin the survey process.

No investigational, experimental, or special procedures were used in the completion of

the project. Each respondent should have only completed the survey once, as addressed

in the informed consent, and the location of completion was up to the respondent. The

survey could have been completed on any computer or mobile device that could access

the survey website.

Data Collection

The survey (Appendix B) was created via the Survey Monkey platform, and covered six

areas: informed consent to participate, the age range treated by the clinician, the type of

licensure of the clinician, the length of time the clinician had been in practice, what

strategies they used to assess for pediatric BPD, and whether they felt a standardized

assessment process would assist them in the assessment and diagnosis of pediatric BPD.

Survey items contained primarily check box answers, and it was estimated that unless a

clinician chose to write in free text, survey completion took about five to ten minutes.

Institutional Review Board approval from California State University, Fresno was

23 obtained. Data was collected from September 13, 2016, through October 12, 2016. No

standardized instruments were used for data collection in this project.

Data Analysis

Emphasis was placed on the descriptive statistics generated from the data

received. This provided information about current practice strategies employed by

clinicians, which substantiated the need for the development of the clinical tool. Three

groupings of variables were subject to statistical analysis. Chi square analysis was

performed on: the age range treated by the clinician and what assessment strategies

employed in practice, length of time in practice and assessment strategies employed in

practice, and level of licensure and assessment strategies employed in practice (Field,

2013a). None of the Chi square analyses resulted in significant findings. However, the

survey data yielded varied assessment and interview strategies (Appendix C).

Potential Benefits

There were no immediate or direct benefits to any respondent who completed the

survey. Any respondent who wishes to receive results of the survey data was provided

information to request this as a part of the informed consent. It was anticipated that

clinicians were likely to see more benefit from the resulting tool that was created, than

from participation in the survey. This tool will guide clinicians through a robust

assessment of possible pediatric BPD, and aid them in more accurately diagnosing this

condition.

Potential Risks

Risks to respondents were minimal for this study. Risks involved the time needed

to complete the survey and any distress that occurred from examining their assessment

24 strategies. There were no social, physical, economic, or legal risks anticipated for any

survey respondent. The clinical tool will be validated as a separate endeavor after

completion of this project and academic program, so there was no risk at this time to any

patient. There were no violations of normal expectations.

Precautions to Minimize Risk

Completion of the survey was voluntary and anonymous. At no point during the

survey was any personally identifying information gathered. The respondents completed

the survey in an electronic format. There were no individual survey tools collected by

any other means, and therefore no physical storage or destruction was necessary. Survey

data is accessed by the investigator on the survey website. This website is username and

password protected, preventing any unauthorized access to survey data. Any physical

data that is printed, and not maintained in an electronic form on the secured website, will

be secured in a locked filing cabinet. Data analysis reports from statistical software are

being stored in a biometrically locked laptop computer.

CHAPTER 4: RESULTS

Data from the clinician survey was analyzed using IBM SPSS, version 23.

Descriptive statistics, and frequencies were obtained in addition to completion of analysis

related to the research questions. Review of the literature yielded information related to

the assessment of pediatric BPD, susceptibility genes related to BPD, and the

neurobiological changes seen in BPD. The information from the literature review, and

data from the clinical survey were combined to guide the development of the clinical

tool.

Results

Sixteen respondents completed the required questions of the survey. Twenty

respondents began the survey; four either did not complete the required questions of the

survey or did not meet inclusion criteria. The sample was comprised of physicians (n=4,

25%), nurse practitioners (n=11, 68.8%), and a clinical nurse specialist (n=1, 6.2%). Half

of these clinicians treated patients across the lifespan (n=8, 50%), while some treated

child and adolescents only (n=6, 37.5%), and the remainder treated children, adolescents,

and young adults (n=2, 12.5%). The length of time these clinicians had been in practice

was also explored. The largest group of respondents had been in practice between six

and ten years (n=7, 43.8%). Other responses included: zero to five years (n=2, 12.5%),

eleven to twenty years (n=3, 18.7%), and twenty-one or more years (n=4, 25%).

Chi Square Analyses

Testing of the aforementioned research questions was completed by

performing Chi square analyses to determine if there were any significant

relationships between the assessment strategies used by clinicians and 1) the level

26

of licensure of the clinician (mood journaling p=0.055, sleep journaling p=0.113,

rating scales p=0.379, lab studies p=0.195, will not diagnose p=0.660), 2) the

length of time the clinician had been in practice (mood journaling p=0.454, sleep

journaling p=0.917, rating scales p=0.450, lab studies p=0.468, will not diagnose

p=0.558), and 3) the age range the clinician treated (mood journaling p=0.558,

sleep journaling p=0.141, rating scales p=0.915, lab studies p=0.641, will not

diagnose p=0.180). None of the Chi square analyses resulted in significant

findings. None of the clinician respondents reported using imaging studies or

genetic testing regularly, so there are no p values for these measures. The

weakness of the sample size may have contributed to the lack of significance in

findings. This should be considered, and more data obtained in the future.

CHAPTER 5: DISCUSSION

Discussion Regarding Assessment Strategies

Overall, clinicians demonstrated consistency in their responses regarding the

symptoms assessed when diagnosing pediatric BPD. Though no statistically significant

findings were found between the assessment strategies used and the clinician survey data,

there was variation seen in the responses to the assessment strategies employed in

practice (see Appendix C, Chart 1). The variation in responses is either random or

related to a variable that was not studied. It is presumed that use of the clinical tool will

help to create greater consistency in the assessment strategies used. The final question of

the survey asked respondents whether or not a valid and reliable assessment tool would

be helpful to them, the majority of respondents (n=14, 87.5%) indicated that this would

be helpful to them. Based on this data obtained from the clinician study, there should be

openness to the diffusion of the tool and adoption of its process.

Data obtained regarding the family of origin showed some variation in responses

as well (see Appendix C, Chart 2), though not as dramatically as the assessment

strategies. A thorough family history should be consistently obtained due to the

heritability of BPD (Lichtenstein et al., 2009). The significance of these particular

aspects of family history are important in the assessment of pediatric BPD, further

consistency in this area of assessment could yield more effective diagnostics. Sleep

disturbance is a common symptom of BPD. Exploring patterns of this occurring in the

family of origin can be helpful in identifying BPD in the patient; this response showed

the greatest variation in responses in this section of questions.

28 Clinicians were given the opportunity to provide free text responses regarding

how they distinguish between the aforementioned conditions that have similar symptoms

to pediatric BPD. The common themes contained in the responses received for this

question (n=10) included assessing for sleep disturbances, manic or grandiose periods,

and thorough assessment. One clinician responded that they would refer out any child or

adolescent that they suspected had BPD. Another free text question asked clinicians to

explain their perspective if they would not diagnose BPD in a child or adolescent. Two

clinicians created responses for this question, and both indicated that the clinician would

diagnose BPD in an adolescent if they met diagnostic criteria, but would not diagnose

BPD in a child. This question also did not require a response of the respondents.

Project Outcomes

A clinical tool has been created (see Appendix D) to aid in the assessment and

diagnosis of pediatric BPD. This tool has been created by synthesizing the data obtained

through the clinician survey, the information obtained during the literature review, and

the clinical knowledge of the author. The clinical tool is designed to be used in the

mental health setting, and could also be used in the primary care setting as a means of

determining when to refer for specialty assessment.

The clinical tool provides a comprehensive checklist of symptoms and prompts

the clinician to have the patient to mood journal. After this, the tool guides the clinician

to have the patient or their family to complete rating scales. Though any reliable and

validated screening tool is acceptable, information regarding the FIRM (Algorta et al.,

2013), and the Child Mania Rating Scale – Parent Version (CMRS-P) (Pavuluri, Henry,

Devineni, Carbray, & Birmaher, 2006) are included. Permission exists for the FIRM in

29 academic and research contexts. The CMRS-P is available for download on the internet,

and permission for use was separately obtained by the author (Appendix E). If pediatric

BPD is still suspected, further evaluation is recommended. Laboratory studies are

recommended to rule out any underlying medical comorbidities that may contribute to the

clinical presentation; these would also allow for baseline levels to be obtained should

pharmacologic management commence in the future. Though the laboratory tests

ordered should be based upon the assessment of the clinician, some routine

recommendations to consider are: complete blood count with differential, comprehensive

metabolic panel, lipid panel, glycosylated hemoglobin, and thyroid stimulating hormone.

Other tests that may be warranted based on the individual patient presentation might

include: urine drug screen, urine human chorionic gonadotropin, prolactin, and vitamin

D. Testing for methylenetetrahydrofolate reductase (MTHFR) polymorphisms should be

considered on a case by case basis, as MTHFR polymorphisms are associated with mood

struggles, although this is not diagnostic of BPD (Gilbody, Lewis, & Lightfoot, 2007). It

is possible that with this level of thorough assessment, BPD could be ruled in or out.

However, if the clinical picture remains uncertain, MRI studies should be considered to

assess for neurobiological changes. Current research suggests that changes can be found

in the scans of BPD patients; particular consistency has been noted in changes in GMV

(James et al., 2011).

Validation of this screening tool will be completed in the future. After validity

and reliability have been established, broader dissemination, publication, and training

regarding the use of the tool will occur. It is hoped that the use of this tool will provide a

standardized platform for the assessment and diagnosis of BPD, and help to create greater

30 diagnostic accuracy. It is anticipated that the tool will be available initially in pen and

paper format, and eventually developed into a smartphone application. Use of this tool

will provide an innovative approach to assessment, that will enhance the efficiency and

effectiveness of assessment. These attributes of the tool will be addressed during training

to aid in diffusion and adoption of the tool concepts.

Limitations

Crede (2010) reported the effects of random responding to the validity of

psychological tests and in research. The author noted that random responding could lead

to erroneous correlational relationships being identified. The converse could also be true,

that relationships that would have appeared stronger had the responses not been random

will not be identified. It is unknown if the effects of random sampling contributed to the

results of this project, further research is needed.

A low response rate from clinicians was another limitation of this project.

Cunningham, et al. (2015) noted that physicians are typically low responders to survey

research. The authors conducted survey research of various types of physicians to look at

response rates. Psychiatrists had by far the lowest return rate, and this was with a

supported, advertised, and structured dissemination of the survey (Cunningham et al.,

2015).

A perceived bias of this project could be that the clinician survey was

disseminated to many professional contacts of the author. However, these contacts

allowed the survey to reach several large university medical centers, several university

systems, the Ministry of Health in Singapore, several psychiatric hospitals, and a large

medical group. Additionally, a past president of the Northern California Regional

31 Organization of Child and Adolescent Psychiatry was able to disseminate the survey to

clinician members. Unfortunately, despite these seeming far-reaching contacts, very few

surveys were completed.

Recommendations for Further Study

Mental health providers like psychologists, therapists, and social workers can

diagnose pediatric BPD. These clinicians cannot order imaging studies or laboratory

studies, however, and as such, they were not included in this initial clinician survey.

They should be included in any future clinician surveys to understand their assessment

strategies, and to help garner more robust data. Due to the low number of clinician

respondents, continued study of clinician practices would be useful to see if any statistical

significance could be obtained and to re-enforce the findings that were discovered.

The most recent edition of the Diagnostic and Statistical Manual of Mental

Disorders (DSM-5) brought updates to many pediatric mental health conditions. The

DSM-5 provides support for the diagnosis of pediatric BPD when the appropriate

symptomatology exists (American Psychiatric Association, 2013). One diagnostic

addition to the DSM-5 was that of disruptive mood dysregulation disorder (DMDD)

(American Psychiatric Association, 2013). This diagnosis captures many of the children

and adolescents that might have previously been mislabeled as having BPD. This is

considered a depressive disorder, however, not a cycling mood disorder like BPD.

Irritability in children and adolescents is a hallmark feature of both conditions. However,

a distinguishing factor is that the irritability in DMDD is persistently irritable, and in

BPD there will be periods of irritability followed by other distinguishable mood states

(American Psychiatric Association, 2013). Stringaris et al. (2010) noted that youth with

32 severe mood dysregulation, as is seen in DMDD are very unlikely to develop a mixed or

manic episode. This type of episode would be seen relatively commonly in the BPD

population. Additionally, neurobiological differences can be appreciated in the brains of

patients with severe mood dysregulation, like DMDD, as compared to those with BPD,

when given the same tasks to complete (Adleman et al., 2011).

Ensuring that the clinical tool is sensitive to BPD is important. This will help

reduce misdiagnosis of other similarly presenting conditions like DMDD, ODD, CD, and

ADHD. This consideration is one reason that the FIRM was selected as one of the

recommended screening methods within the clinical tool. Research has shown that the

FIRM was more sensitive to BPD than other available scales, and was not sensitive to

ADHD (Algorta et al., 2013). The clinical tool now needs to be validated before

disseminating it into clinical practice. This is a crucial next research step to allow this

project to proceed.

Healthcare Improvement

Creating consistency in the evaluation of pediatric BPD will help to ensure that

the disorder is more accurately diagnosed. A more robust evaluation process will likely

help parents of potential BPD patients to be more accepting of the diagnosis, and thereby

help ensure early treatment. Early identification and treatment will help lead to more

positive outcomes for this vulnerable population (Maniscalco & Hamrin, 2008). The

intent is for this clinical tool to reach beyond psychiatry, and into primary care as well.

The assessment strategies will be clearly defined enough that those working in primary

care would be comfortable completing the assessment, and referring for treatment if a

diagnosis of BPD is likely.

33 Conclusion

The development of the clinical tool provides a model for assessment that

can be used to diagnose BPD in the pediatric population. Data shows that the

incidence of the pediatric BPD has been rising (Littrell & Lyons, 2010). Current

literature has demonstrated that there is evidence for biological and genetic

changes that can be seen in the BPD patient, and the incorporation of the

expanding field of science into diagnostic practices is warranted. Clinician survey

data demonstrated that while clinicians seem to be consistent in their assessment

of symptoms of BPD, there is inconsistency in the use of other screening

strategies. Ultimately, the majority of clinician respondents indicated that a valid

and reliable clinical tool would be helpful to them professionally. This project

seeks to provide such a tool, and it is hoped that broad diffusion and adoption of

this tool will help to improve the care and outcomes of child and adolescent

patients everywhere.

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APPENDICES

APPENDIX A: GLOSSARY OF TERMS

45

Term Abbreviation

Analysis of Variance ANOVA

Attetion Deficit Hyperactivity Disorder ADHD

Bipolar Disorder BPD

Brain-derived Neurotrophic Factor BDNF

Calcium/Calmodulin Dependent Protein Kinase Kinase 2 CAMKK2

Catechol-O-Methyltransferase COMT

Child Behavior Checklist CBCL

Child Mania Rating Scale – Parent Version CMRS-P

Children’s Global Assessment Scale CGAS

Conduct Disorder CD

Diagnostic Interview for Children and Adolescents – Parent

Version

DICA-P

Diagnostic and Statistical Manual of Mental Disorders, 5th

Edition

DSM-5

Disruptive Mood Dysregulation Disorder DMDD

Dopamine Transporter DAT

Family Index of Risk for Mood Disorders FIRM

46

Gray Matter Volume GMV

Hamilton Rating Scale for Depression HAM-D

Kiddie Schedule for Affective Disorders and Schizophrenia K-SADS

Kiddie Schedule for Affective Disorders and Schizophrenia

- Epidemiologic

K-SADS-E

Kiddie Schedule for Affective Disorders and Schizophrenia – Mania Rating Scale KMRS

Kiddie Schedule for Affective Disorders and Schizophrenia – Present and Lifetime K-SADS-PL

Magnetic Resonance Imaging MRI

Methylenetetrahydrofolate Reductase MTHFR

Mini International Neuropsychiatric Interview MINI

Mood Disorder Questionnaire - Parent PMD-Q

Oppositional Defiant Disorder ODD

Purinergic Receptor P2X 4 P2RX4

Purinergic Receptor P2X 7 P2RX7

Single Nucleotide Polymorphism SNP

Structured Clinical Interview for DSM-IV SCID

Toll-like Receptor 2 TLR2

47

Transient Receptor Potential Cation Channel Subfamily M

Member 2

TRPM2

Unipolar Depression UD

Young Mania Rating Scale YMRS

APPENDIX B: CLINICIAN SURVEY

49

Appendix B – Clinician Survey

50

51

52

53

54

APPENDIX C: CLINICIAN DATA TABLES

56

Appendix C – Clinician Data Charts

Chart 1 – Assessment Strategies Employed

Chart 2 – Family Screening

0

2

4

6

8

10

12

14

16

Mood Journaling Sleep Journaling Rating Scales Lab Tests Will Not Dx

Assessment Strategies Employed

Yes No

0

2

4

6

8

10

12

14

16

Psychiatric Dx in Family Substance Abuse in Family Insomnia in Family Completed or AttemptedSuicide in Family

Family Screening

Most of the time Occasionally Rarely

APPENDIX D: CLINICAL TOOL

58

Appendix D – Clinical Tool

59

60

61

62

63

64

65

APPENDIX E: PERMISSION FOR USE

67

Appendix E – Permission for Use